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Subcellular fractionation of Streptococcus pyogenes seotype M1

ABSTRACT: This data presents the complete proteomic subcellular characterization (extracellular secreted proteins, cell wall-associated proteins, cytosolic proteins, crude membrane proteins, peripheral membrane proteins and proteins present in purified membranes) of Streptococcus pyogenes serotype M1 (strain AP1).

INSTRUMENT(S): Q Exactive

ORGANISM(S): Streptococcus Pyogenes Serotype M1 (ncbitaxon:301447)

SUBMITTER: Lotta Happonen

PROVIDER: MSV000080971 | MassIVE | Thu Apr 20 06:50:00 BST 2017

SECONDARY ACCESSION(S): PXD006345

REPOSITORIES: MassIVE

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Project description:Streptococcus pyogenes is a major causative agent of tonsillitis or pharyngitis in children, which can lead to more invasive infections and noninfectious sequellae. S. pyogenes can persist in tonsils, while one-third of children treated with antibiotics continue to shed streptococci and have recurrent infections. Mouse nasal-associated lymphoid tissue (NALT) is functionally analogous to human oropharangeal lymphoid tissues. The innate immune responses of naÃ¯ve cells from a mucosal site to S. pyogenes is not well described; therefore, we infected C57BL/6 mice intranasally with 108 CFU S. pyogenes. Transcriptional responses by NALT after S. pyogenes infection were analyzed by Affymetrix microarray and quantitative RT-PCR. Wild-type S. pyogenes induces transcription of both type I and IFN-gamma-responsive genes, pro-inflammatory genes, and acute phase response plasma proteins within 24h after infection. Invasion of NALT and the induction of the interferon response were not dependent on expression of anti-phagocytic M1 protein. However, infection with an attenuated, less invasive mutant indicated that a robust innate response by NALT is significantly influenced by intra-NALT bacterial load. Granulocytic populations of NALT, cervical lymph nodes and spleen were discriminated by characteristic surface and intracellular markers. Intranasal infection induces systemic release of neutrophils and a substantial influx of neutrophils into NALT at 24h, which decline by 48h after infection. Macrophages do not significantly increase in S. pyogenes-infected NALT. Intranasal infection of IFN-gamma -/- (GKO) C57BL/6 mice did not lead to systemic dissemination of wild type S. pyogenes, despite reduced expression of IFN-gamma-responsive mRNAs in NALT. Infected GKO mice had an unregulated influx of neutrophils into NALT compared to immunocompetant mice and mice treated with an anti-IFN-gamma antibody more rapidly cleared S. pyogenes from NALT. Thus, IFN-gamma-induced responses have a suppressive influence on early clearance of this pathogen from NALT. Experiment Overall Design: C57BL/6 mice (6-10 weeks old), 4 per group, were infected intranasally with log-phase Streptococcus pyogenes, 2 to 4 x 10^8 CFU per 15 Âµl of pyrogen-free PBS. Sham-infected mice were administered 15 Âµl of the same PBS. Mice were infected with wild type strain 90-226 (Cue 1998), a 90-226 strain containing an in-frame deletion of M1 protein (90-226 delta emm1) (Zimmerlein 2005) or an attenuated 90-226 which lacks both M1 and SCPA proteins (90-226att). NALT was collected from mice at 24h after infection and stored in RNAlater until RNA could be purified).

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Subcellular fractionation of Streptococcus pyogenes seotype M1

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